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经验公式(希尔记法):
C18H10F3NO3S2
化学文摘社编号:
分子量:
409.40
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
CFTR(inh)-172, ≥98% (HPLC), powder
SMILES string
OC(=O)c1ccc(cc1)\C=C2\SC(=S)N(C2=O)c3cccc(c3)C(F)(F)F
InChI key
JIMHYXZZCWVCMI-RIYZIHGNSA-N
InChI
1S/C18H10F3NO3S2/c19-18(20,21)12-2-1-3-13(9-12)22-15(23)14(27-17(22)26)8-10-4-6-11(7-5-10)16(24)25/h1-9H,(H,24,25)/b14-8+
assay
≥98% (HPLC)
form
powder
color
yellow
solubility
DMSO: ≥10 mg/mL
H2O: insoluble
storage temp.
2-8°C
Quality Level
Application
CFTR(inh)-172用于特异性抑制囊性纤维化跨膜电导调节因子(CFTR)的活性。也可用作 CFTR抑制剂 Inh-172处理福司柯林(毛喉素)和IBMX。
Biochem/physiol Actions
CFTR (inh)-172 是囊性纤维化跨膜传导调节因子 (CFTR) 的抑制剂。
CFTR (inh)-172 是囊性纤维化跨膜传导调节因子 (CFTR) 的抑制剂。K i = 300 nM。CFTR (inh)-172 导致快速、可逆和非电压依赖性抑制;为动物止泻药。CTFR (inh)-172 可能是研究霍乱和其他分泌性腹泻囊性纤维化和肠液丢失动物模型的有用工具。CTFR (inh)-172 在结构上与已知的非特异性 CFTR 抑制剂 DPC,NPPB(货号N4779)和格列本脲。
存储类别
11 - Combustible Solids
wgk
WGK 3
ppe
dust mask type N95 (US), Eyeshields, Faceshields, Gloves
Electrophysiological evaluation of cystic fibrosis conductance transmembrane regulator (CFTR) expression in human monocytes
Ettorre M, et al.
Biochimica et biophysica acta. General subjects, 1840(10), 3088-3095 (2014)
An unexpected effect of TNF-alpha on F508del-CFTR maturation and function
Bitam S, et al.
F1000Research, 4 (2015)
Defective CFTR expression and function are detectable in blood monocytes: development of a new blood test for cystic fibrosis
Sorio C, et al.
Testing, 6(7), e22212-e22212 (2011)
N D Sonawane et al.
Journal of pharmaceutical sciences, 94(1), 134-143 (2005-03-12)
A small-molecule inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR), 3-[(3-trifluoromethyl)phenyl]-5-[(4-carboxyphenyl)methylene]-2-thioxo-4-thiazolidinone (CFTR(inh)-172), reduces enterotoxin-induced intestinal fluid secretion in rodents. Here, we study CFTR(inh)-172 pharmacology and antidiarrheal efficacy in rodents using (14)C-labeled CFTR(inh)-172, liquid chromatography/mass spectrometry, and a closed intestinal
Jinxue Ruan et al.
Molecular therapy. Nucleic acids, 16, 73-81 (2019-03-11)
Cystic fibrosis (CF) is a lethal autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Nuclease-mediated precise gene editing (PGE) represents a promising therapy for CF, for which an efficient strategy that is free
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